Mechanisms of M2 Macrophage-Derived Exosomal Long Non-coding RNA PVT1 in Regulating Th17 Cell Response in Experimental Autoimmune Encephalomyelitisa (Retracted Article)
Long non-coding RNA (lncRNA) is pivotal for multiple sclerosis (MS), but the potential mechanism of lncRNA PVT1 in MS animal model, experimental autoimmune encephalomyelitis (EAE) still remains unclear. In this study, macrophages were firstly isolated and induced to polarize into M2 macrophages. M2...
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| Veröffentlicht in: | Frontiers in immunology 2020-09, Vol.11, p.1934, Article 1934 |
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| description | Long non-coding RNA (lncRNA) is pivotal for multiple sclerosis (MS), but the potential mechanism of lncRNA PVT1 in MS animal model, experimental autoimmune encephalomyelitis (EAE) still remains unclear. In this study, macrophages were firstly isolated and induced to polarize into M2 macrophages. M2 macrophage-derived exosomes (M2-exos) were extracted and identified, and EAE mouse model was established and treated with M2-exos. The effect of M2-exos on EAE mice was evaluated by clinical scores. The proportion of Treg and Th17 cells in spinal cord cells and splenocytes, and levels of inflammatory factors were measured. The targeting relationships among PVT1, miR-21-5p, and SOCS5 were verified. The expression of JAKs/STAT3 pathway-related proteins was measured. After M2-exo treatment, the clinical score of EAE mice decreased, and demyelination and inflammatory infiltration improved; Th17 cells decreased, Treg cells increased, and the levels of inflammatory factors decreased significantly. SOCS5 and PVT1 were downregulated and miR-21-5p was upregulated in EAE mice. PVT1 could sponge miR-21-5p to regulate SOCS5. SOCS5 alleviated EAE symptoms by repressing the JAKs/STAT3 pathway. Together, M2-exos-carried lncRNA PVT1 sponged miR-21-5p to upregulate SOCS5 and inactivate the JAKs/STAT3 pathway, thus reducing inflammation and protecting EAE mice. This study may offer novel treatments for MS. |
| doi_str_mv | 10.3389/fimmu.2020.01934 |
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In this study, macrophages were firstly isolated and induced to polarize into M2 macrophages. M2 macrophage-derived exosomes (M2-exos) were extracted and identified, and EAE mouse model was established and treated with M2-exos. The effect of M2-exos on EAE mice was evaluated by clinical scores. The proportion of Treg and Th17 cells in spinal cord cells and splenocytes, and levels of inflammatory factors were measured. The targeting relationships among PVT1, miR-21-5p, and SOCS5 were verified. The expression of JAKs/STAT3 pathway-related proteins was measured. After M2-exo treatment, the clinical score of EAE mice decreased, and demyelination and inflammatory infiltration improved; Th17 cells decreased, Treg cells increased, and the levels of inflammatory factors decreased significantly. SOCS5 and PVT1 were downregulated and miR-21-5p was upregulated in EAE mice. PVT1 could sponge miR-21-5p to regulate SOCS5. SOCS5 alleviated EAE symptoms by repressing the JAKs/STAT3 pathway. Together, M2-exos-carried lncRNA PVT1 sponged miR-21-5p to upregulate SOCS5 and inactivate the JAKs/STAT3 pathway, thus reducing inflammation and protecting EAE mice. This study may offer novel treatments for MS.</description><identifier>ISSN: 1664-3224</identifier><identifier>EISSN: 1664-3224</identifier><identifier>DOI: 10.3389/fimmu.2020.01934</identifier><identifier>PMID: 33013847</identifier><language>eng</language><publisher>LAUSANNE: Frontiers Media Sa</publisher><subject>Animals ; Cells, Cultured ; Encephalomyelitis, Autoimmune, Experimental - genetics ; Encephalomyelitis, Autoimmune, Experimental - immunology ; Encephalomyelitis, Autoimmune, Experimental - metabolism ; Encephalomyelitis, Autoimmune, Experimental - therapy ; exosomes ; Exosomes - genetics ; Exosomes - metabolism ; Exosomes - transplantation ; experimental autoimmune encephalomyelitis ; Immunology ; Janus Kinases - metabolism ; Life Sciences & Biomedicine ; long non-coding RNA PVT1 ; M2 macrophages ; Macrophages, Peritoneal - metabolism ; Macrophages, Peritoneal - transplantation ; Mice ; Mice, Inbred C57BL ; microRNA-21-5p ; MicroRNAs - genetics ; MicroRNAs - metabolism ; Phenotype ; RNA, Long Noncoding - genetics ; RNA, Long Noncoding - metabolism ; Science & Technology ; Signal Transduction ; SOCS5 ; Spinal Cord - immunology ; Spinal Cord - metabolism ; Spleen - immunology ; Spleen - metabolism ; STAT3 Transcription Factor - metabolism ; Suppressor of Cytokine Signaling Proteins - genetics ; Suppressor of Cytokine Signaling Proteins - metabolism ; T-Lymphocytes, Regulatory - immunology ; T-Lymphocytes, Regulatory - metabolism ; Th17 Cells - immunology ; Th17 Cells - metabolism</subject><ispartof>Frontiers in immunology, 2020-09, Vol.11, p.1934, Article 1934</ispartof><rights>Copyright © 2020 Wu, Xia, Li, Kang, Fang and Huang.</rights><rights>Copyright © 2020 Wu, Xia, Li, Kang, Fang and Huang. 2020 Wu, Xia, Li, Kang, Fang and Huang</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>true</woscitedreferencessubscribed><woscitedreferencescount>31</woscitedreferencescount><woscitedreferencesoriginalsourcerecordid>wos000573636200001</woscitedreferencesoriginalsourcerecordid><cites>FETCH-LOGICAL-d332t-7d71e8ea284c6ff71e6f88b7bbf565bba0949c6f8ed649eeef17a9140587d4403</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC7500097/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC7500097/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,315,728,781,785,865,886,2103,2115,27928,27929,28252,53795,53797</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/33013847$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Wu, Lei</creatorcontrib><creatorcontrib>Xia, Jinjin</creatorcontrib><creatorcontrib>Li, Donghui</creatorcontrib><creatorcontrib>Kang, Ying</creatorcontrib><creatorcontrib>Fang, Wei</creatorcontrib><creatorcontrib>Huang, Peng</creatorcontrib><title>Mechanisms of M2 Macrophage-Derived Exosomal Long Non-coding RNA PVT1 in Regulating Th17 Cell Response in Experimental Autoimmune Encephalomyelitisa (Retracted Article)</title><title>Frontiers in immunology</title><addtitle>FRONT IMMUNOL</addtitle><addtitle>Front Immunol</addtitle><description>Long non-coding RNA (lncRNA) is pivotal for multiple sclerosis (MS), but the potential mechanism of lncRNA PVT1 in MS animal model, experimental autoimmune encephalomyelitis (EAE) still remains unclear. In this study, macrophages were firstly isolated and induced to polarize into M2 macrophages. M2 macrophage-derived exosomes (M2-exos) were extracted and identified, and EAE mouse model was established and treated with M2-exos. The effect of M2-exos on EAE mice was evaluated by clinical scores. The proportion of Treg and Th17 cells in spinal cord cells and splenocytes, and levels of inflammatory factors were measured. The targeting relationships among PVT1, miR-21-5p, and SOCS5 were verified. The expression of JAKs/STAT3 pathway-related proteins was measured. After M2-exo treatment, the clinical score of EAE mice decreased, and demyelination and inflammatory infiltration improved; Th17 cells decreased, Treg cells increased, and the levels of inflammatory factors decreased significantly. SOCS5 and PVT1 were downregulated and miR-21-5p was upregulated in EAE mice. PVT1 could sponge miR-21-5p to regulate SOCS5. SOCS5 alleviated EAE symptoms by repressing the JAKs/STAT3 pathway. Together, M2-exos-carried lncRNA PVT1 sponged miR-21-5p to upregulate SOCS5 and inactivate the JAKs/STAT3 pathway, thus reducing inflammation and protecting EAE mice. This study may offer novel treatments for MS.</description><subject>Animals</subject><subject>Cells, Cultured</subject><subject>Encephalomyelitis, Autoimmune, Experimental - genetics</subject><subject>Encephalomyelitis, Autoimmune, Experimental - immunology</subject><subject>Encephalomyelitis, Autoimmune, Experimental - metabolism</subject><subject>Encephalomyelitis, Autoimmune, Experimental - therapy</subject><subject>exosomes</subject><subject>Exosomes - genetics</subject><subject>Exosomes - metabolism</subject><subject>Exosomes - transplantation</subject><subject>experimental autoimmune encephalomyelitis</subject><subject>Immunology</subject><subject>Janus Kinases - metabolism</subject><subject>Life Sciences & Biomedicine</subject><subject>long non-coding RNA PVT1</subject><subject>M2 macrophages</subject><subject>Macrophages, Peritoneal - metabolism</subject><subject>Macrophages, Peritoneal - transplantation</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>microRNA-21-5p</subject><subject>MicroRNAs - genetics</subject><subject>MicroRNAs - metabolism</subject><subject>Phenotype</subject><subject>RNA, Long Noncoding - genetics</subject><subject>RNA, Long Noncoding - metabolism</subject><subject>Science & Technology</subject><subject>Signal Transduction</subject><subject>SOCS5</subject><subject>Spinal Cord - immunology</subject><subject>Spinal Cord - metabolism</subject><subject>Spleen - immunology</subject><subject>Spleen - metabolism</subject><subject>STAT3 Transcription Factor - metabolism</subject><subject>Suppressor of Cytokine Signaling Proteins - genetics</subject><subject>Suppressor of Cytokine Signaling Proteins - metabolism</subject><subject>T-Lymphocytes, Regulatory - immunology</subject><subject>T-Lymphocytes, Regulatory - metabolism</subject><subject>Th17 Cells - immunology</subject><subject>Th17 Cells - metabolism</subject><issn>1664-3224</issn><issn>1664-3224</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2020</creationdate><recordtype>article</recordtype><sourceid>AOWDO</sourceid><sourceid>EIF</sourceid><sourceid>DOA</sourceid><recordid>eNqNkU1v1DAQhiMEolXpnRPyEYSy2LETOxekVbqUSrsFrRaukZ2Ms64SO8pHaf8RP7OzLFTtDV88Hr9-ZjxvFL1ldMG5yj9Z13XzIqEJXVCWc_EiOmVZJmKeJOLlk_gkOh_HG4pL5Jzz9HV0wjllXAl5Gv3eQLXX3o3dSIIlm4RsdDWEfq8biC9gcLdQk9VdGEOnW7IOviHXwcdVqB2G2-sl-f5zx4jzZAvN3OrpkN7tmSQFtC0mxz74EQ6C1V2PvA78hKTlPIVD_x7IyleA9drQ3UPrJjdq8n4L06CrCWsvh8lVLXx4E72yuh3h_O9-Fv34stoVX-P1t8urYrmOa86TKZa1ZKBAJ0pUmbV4yKxSRhpj0yw1RtNc5HijoM5EDgCWSZ0zQVMlayEoP4uujtw66Juyx4b1cF8G7co_iTA0pT62VIIRQLnR1uAsmcoVr2qWKIugTGaUI-vzkdXPpoO6wq8Pun0GfX7j3b5swm0pU3Qrlwh49xTw-PKffyj4eBT8AhPsWDnAYT7KEJJKnvEsObjPUK3-X124Cd0Mvgizn_gDyBfB9w</recordid><startdate>20200904</startdate><enddate>20200904</enddate><creator>Wu, Lei</creator><creator>Xia, Jinjin</creator><creator>Li, Donghui</creator><creator>Kang, Ying</creator><creator>Fang, Wei</creator><creator>Huang, Peng</creator><general>Frontiers Media Sa</general><general>Frontiers Media S.A</general><scope>AOWDO</scope><scope>BLEPL</scope><scope>DTL</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>5PM</scope><scope>DOA</scope></search><sort><creationdate>20200904</creationdate><title>Mechanisms of M2 Macrophage-Derived Exosomal Long Non-coding RNA PVT1 in Regulating Th17 Cell Response in Experimental Autoimmune Encephalomyelitisa (Retracted Article)</title><author>Wu, Lei ; Xia, Jinjin ; Li, Donghui ; Kang, Ying ; Fang, Wei ; Huang, Peng</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-d332t-7d71e8ea284c6ff71e6f88b7bbf565bba0949c6f8ed649eeef17a9140587d4403</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2020</creationdate><topic>Animals</topic><topic>Cells, Cultured</topic><topic>Encephalomyelitis, Autoimmune, Experimental - genetics</topic><topic>Encephalomyelitis, Autoimmune, Experimental - immunology</topic><topic>Encephalomyelitis, Autoimmune, Experimental - metabolism</topic><topic>Encephalomyelitis, Autoimmune, Experimental - therapy</topic><topic>exosomes</topic><topic>Exosomes - genetics</topic><topic>Exosomes - metabolism</topic><topic>Exosomes - transplantation</topic><topic>experimental autoimmune encephalomyelitis</topic><topic>Immunology</topic><topic>Janus Kinases - metabolism</topic><topic>Life Sciences & Biomedicine</topic><topic>long non-coding RNA PVT1</topic><topic>M2 macrophages</topic><topic>Macrophages, Peritoneal - metabolism</topic><topic>Macrophages, Peritoneal - transplantation</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>microRNA-21-5p</topic><topic>MicroRNAs - genetics</topic><topic>MicroRNAs - metabolism</topic><topic>Phenotype</topic><topic>RNA, Long Noncoding - genetics</topic><topic>RNA, Long Noncoding - metabolism</topic><topic>Science & Technology</topic><topic>Signal Transduction</topic><topic>SOCS5</topic><topic>Spinal Cord - immunology</topic><topic>Spinal Cord - metabolism</topic><topic>Spleen - immunology</topic><topic>Spleen - metabolism</topic><topic>STAT3 Transcription Factor - metabolism</topic><topic>Suppressor of Cytokine Signaling Proteins - genetics</topic><topic>Suppressor of Cytokine Signaling Proteins - metabolism</topic><topic>T-Lymphocytes, Regulatory - immunology</topic><topic>T-Lymphocytes, Regulatory - metabolism</topic><topic>Th17 Cells - immunology</topic><topic>Th17 Cells - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Wu, Lei</creatorcontrib><creatorcontrib>Xia, Jinjin</creatorcontrib><creatorcontrib>Li, Donghui</creatorcontrib><creatorcontrib>Kang, Ying</creatorcontrib><creatorcontrib>Fang, Wei</creatorcontrib><creatorcontrib>Huang, Peng</creatorcontrib><collection>Web of Science - Science Citation Index Expanded - 2020</collection><collection>Web of Science Core Collection</collection><collection>Science Citation Index Expanded</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>PubMed Central (Full Participant titles)</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>Frontiers in immunology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Wu, Lei</au><au>Xia, Jinjin</au><au>Li, Donghui</au><au>Kang, Ying</au><au>Fang, Wei</au><au>Huang, Peng</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Mechanisms of M2 Macrophage-Derived Exosomal Long Non-coding RNA PVT1 in Regulating Th17 Cell Response in Experimental Autoimmune Encephalomyelitisa (Retracted Article)</atitle><jtitle>Frontiers in immunology</jtitle><stitle>FRONT IMMUNOL</stitle><addtitle>Front Immunol</addtitle><date>2020-09-04</date><risdate>2020</risdate><volume>11</volume><spage>1934</spage><pages>1934-</pages><artnum>1934</artnum><issn>1664-3224</issn><eissn>1664-3224</eissn><abstract>Long non-coding RNA (lncRNA) is pivotal for multiple sclerosis (MS), but the potential mechanism of lncRNA PVT1 in MS animal model, experimental autoimmune encephalomyelitis (EAE) still remains unclear. In this study, macrophages were firstly isolated and induced to polarize into M2 macrophages. M2 macrophage-derived exosomes (M2-exos) were extracted and identified, and EAE mouse model was established and treated with M2-exos. The effect of M2-exos on EAE mice was evaluated by clinical scores. The proportion of Treg and Th17 cells in spinal cord cells and splenocytes, and levels of inflammatory factors were measured. The targeting relationships among PVT1, miR-21-5p, and SOCS5 were verified. The expression of JAKs/STAT3 pathway-related proteins was measured. After M2-exo treatment, the clinical score of EAE mice decreased, and demyelination and inflammatory infiltration improved; Th17 cells decreased, Treg cells increased, and the levels of inflammatory factors decreased significantly. SOCS5 and PVT1 were downregulated and miR-21-5p was upregulated in EAE mice. PVT1 could sponge miR-21-5p to regulate SOCS5. SOCS5 alleviated EAE symptoms by repressing the JAKs/STAT3 pathway. Together, M2-exos-carried lncRNA PVT1 sponged miR-21-5p to upregulate SOCS5 and inactivate the JAKs/STAT3 pathway, thus reducing inflammation and protecting EAE mice. This study may offer novel treatments for MS.</abstract><cop>LAUSANNE</cop><pub>Frontiers Media Sa</pub><pmid>33013847</pmid><doi>10.3389/fimmu.2020.01934</doi><tpages>14</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Animals Cells, Cultured Encephalomyelitis, Autoimmune, Experimental - genetics Encephalomyelitis, Autoimmune, Experimental - immunology Encephalomyelitis, Autoimmune, Experimental - metabolism Encephalomyelitis, Autoimmune, Experimental - therapy exosomes Exosomes - genetics Exosomes - metabolism Exosomes - transplantation experimental autoimmune encephalomyelitis Immunology Janus Kinases - metabolism Life Sciences & Biomedicine long non-coding RNA PVT1 M2 macrophages Macrophages, Peritoneal - metabolism Macrophages, Peritoneal - transplantation Mice Mice, Inbred C57BL microRNA-21-5p MicroRNAs - genetics MicroRNAs - metabolism Phenotype RNA, Long Noncoding - genetics RNA, Long Noncoding - metabolism Science & Technology Signal Transduction SOCS5 Spinal Cord - immunology Spinal Cord - metabolism Spleen - immunology Spleen - metabolism STAT3 Transcription Factor - metabolism Suppressor of Cytokine Signaling Proteins - genetics Suppressor of Cytokine Signaling Proteins - metabolism T-Lymphocytes, Regulatory - immunology T-Lymphocytes, Regulatory - metabolism Th17 Cells - immunology Th17 Cells - metabolism |
| title | Mechanisms of M2 Macrophage-Derived Exosomal Long Non-coding RNA PVT1 in Regulating Th17 Cell Response in Experimental Autoimmune Encephalomyelitisa (Retracted Article) |
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